Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Nascent RNA antagonises the interaction of a set of regulatory proteins with chromatin

ABSTRACT: A number of regulatory factors are recruited to chromatin by specialised RNAs. Whether RNA has a more general role in regulating the interaction of proteins with chromatin has not been determined. We used proteomics methods to measure the global impact of nascent RNA on chromatin in embryonic stem cells. Surprisingly, we found that nascent RNA primarily antagonised the interaction of chromatin modifiers and transcriptional regulators with chromatin. Transcriptional inhibition and RNA degradation induced recruitment of a set of transcriptional regulators, chromatin modifiers, nucleosome remodelers, and regulators of higher-order structure. RNA directly bound to factors including BAF, NuRD, EHMT1 and INO80 and inhibited their interaction with nucleosomes. The transcriptional elongation factor P-TEFb directly bound pre-mRNA and its recruitment to chromatin upon Pol II inhibition was regulated by the 7SK ribonucleoprotein complex. We postulate that by antagonising the interaction of regulatory proteins with chromatin, nascent RNA links transcriptional output with chromatin composition.

ORGANISM(S): Mus musculus

PROVIDER: GSE150677 | GEO | 2021/06/23

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Similar Datasets

Nascent RNA antagonises the interaction of regulatory proteins with chromatin

Project description:A number of transcriptional and chromatin regulatory proteins have been reported to be recruited to chromatin by specific regulatory RNAs. Whether RNA has a more general role in the interaction of proteins with chromatin is unknown. We used proteomics methods to determine the global impact of nascent RNA on chromatin in embryonic stem cells. Surprisingly, we found that nascent RNA primarily antagonises the interaction of chromatin modifiers and transcriptional regulators with chromatin. Transcriptional inhibition and RNA degradation induced recruitment of a set of transcriptional regulators, chromatin modifiers, nucleosome remodelers, and regulators of higher-order structure. RNA directly bound to factors including BAF, NuRD, EHMT1 and INO80 and inhibited their interaction with nucleosomes. In the case of the transcriptional elongation factor P-TEFb, direct binding to pre-mRNA released it from the chromatin-associated 7SK ribonucleoprotein complex. We propose that through these mechanisms, nascent RNA provides a direct link between transcriptional output and chromatin state.

2021-06-15 | PXD018706 | Pride

Nascent RNA antagonises the interaction of a set of regulatory proteins with chromatin

Project description:Nascent RNA antagonises the interaction of a set of regulatory proteins with chromatin

| PRJNA633141 | ENA

A novel transcriptional signalling pathway mediated by the trafficking protein Ambra1 via scaffolding Atf2 complexes

Project description:Previously, we reported that Ambra1 is a core component of a cytoplasmic trafficking network, acting as a spatial rheostat to control active Src and FAK levels in addition to its critical roles in autophagy during neurogenesis. Here we identify a novel nuclear scaffolding function for Ambra1 that controls gene expression. Ambra1 binds to nuclear pore proteins, to other adaptor proteins like FAK and Akap8 in the nucleus, as well as to chromatin modifiers and transcriptional regulators such as Brg1, Cdk9 and the cAMP-regulated transcription factor Atf2. Ambra1 contributes to their association with chromatin and we identified genes whose transcription is regulated by Ambra1 complexes, likely via histone modifications and phospho-Atf2-dependent transcription. Therefore, Ambra1 scaffolds protein complexes at chromatin, regulating transcriptional signalling in the nucleus; in particular, it recruits chromatin modifiers and transcriptional regulators to control expression of genes such as Angpt1, Tgfb2, Tgfb3, Itga8 and Itgb7 that likely contribute to the role of Ambra1 in cancer cell invasion.

2021-09-09 | PXD018745 | Pride

Overexpression of c-Myc antagonises transcriptional output of the androgen receptor in prostate cancer [expression]

Project description:Prostate cancer is the most common non-cutaneous cancer in men. The androgen receptor (AR) a ligand-activated transcription factor, constitutes the main drug target for advanced cases of the disease. However, a variety of other transcription factors and signalling networks have been shown to be altered in patients and to influence AR activity. The oncogenic transcription factor c-Myc has been studied extensively in multiple malignancies, but its impact on AR activity in prostate cancer remains elusive. In this study we assessed the impact of clinically relevant levels of c-Myc overexpression on AR activity and transcriptional output. We found that c-Myc and the AR share a substantial amount of binding sites, which exhibit enhancer-like characteristics. Interestingly, c-Myc overexpression altered global AR chromatin occupancy and antagonised a subset of androgen-induced genes. Furthermore, c-Myc overexpression modified histone marks, most notably H3K4me1 and H3K27me3. Lastly, we validated the antagonistic relationship between c-Myc and two AR target genes, KLK3 and GNMT, in patient samples.

2017-04-14 | GSE73917 | GEO

Msx1 ChIP-Seq from C2C12 murine myoblast cells expressing Flag-Msx1 protein

Project description:The spatial and temporal control of gene expression during development requires the concerted actions of sequence-specific transcriptional regulators and epigenetic chromatin modifiers, which are thought to function within precise nuclear compartments. However, how these activities are coordinated within the dynamic context of the nuclear environment is still largely unresolved. Here we show that transcriptional repression by the Msx1 homeoprotein coordinates recruitment of Polycomb to genomic targets with localization to the nuclear periphery. We used genome-wide ChIP-Seq analyses to identify genomic binding sites for Msx1 in C2C12 murine myoblast cells.

2011-08-17 | GSE26711 | GEO

Sox2 is present in RNA binding complexes and interacts with snRNA 7SK in mouse embryonic stem cells

Project description:Sox2 is a master transcriptional regulator of embryonic development and has been found to interact with RNA binding proteins such as the non-coding RNA 7SK. 7SK has been shown to regulate transcription at regulatory regions, which could suggest a functional interaction with Sox2 for chromatin recruitment. In this experiment, we assessed chromatin occupancy of 7SK by Chromatin Isolation by RNA Purification (ChIRP) in Sox2 depleted mES cells and found no evidence of Sox2 modulating recruitment of 7SK to chromatin.

2019-05-07 | E-MTAB-7570 | biostudies-arrayexpress

Tat controls RNA Polymerase II and the epigenetic landscape to precisely rewire cellular transcriptional programs (ChIP-Seq)

Project description:Transcription factors mediate precise regulation of gene expression programs to modulate key biological processes. In addition to controlling HIV transcription, Tat appears to modulate cellular transcription to alter the biology of target immune cells and generate a permissive state for HIV infection. However, the molecular mechanisms of transcriptional control have remained elusive. Here, we identified the direct target genes of Tat using genomics and defined mechanisms by which Tat selectively rewires cellular transcriptional programs. Interestingly, Tat functions as both transcriptional activator and repressor of a defined set of genes sharing functional annotations and regulated by master transcriptional regulators such as T-cell identity factors. Tat is recruited to precise genomic domains (promoters and intragenic enhancers) through interaction with master transcriptional regulators to control both the transcription initiation and elongation steps. Tat mediates transcription initiation by modulating Pol II recruitment to promoters and intragenic enhancers and fine-tuning chromatin looping. Tat stimulates or blocks RNA Polymerase (Pol) II recruitment or promoter-proximal pause release thereby promoting gene activation or repression, respectively. Global analysis of chromatin signatures revealed correlation of transcription activity marks with Pol II recruitment or pause release status at gene promoters and enhancers, and transcription elongation at coding units. We propose that Tat has evolved these unique properties to hijack precise genomic domains to control cellular transcription using unexpected regulatory mechanisms, which showed marked differences to the regulation of the HIV genome. Our studies also reveal that Tat can be used as a molecular probe to decode general principles of transcriptional regulation. ChIP of various DNA binding proteins

2015-06-15 | E-GEOD-65687 | biostudies-arrayexpress

Tat controls RNA Polymerase II and the epigenetic landscape to precisely rewire cellular transcriptional programs (RNA-Seq)

2015-06-15 | E-GEOD-65688 | biostudies-arrayexpress

Overexpression of c-Myc antagonises transcriptional output of the androgen receptor in prostate cancer [ChIP-Seq]

Project description:c-Myc overexpression LNCaP cells were treated with R1881 or R1881+Doxycycline (to induce c-Myc overexpression) and ChIP-seq studies were performed using antibodies against c-Myc, AR, H3K4me1, H3K4me3, H3K27ac and H3K27m3 Prostate cancer is the most common non-cutaneous cancer in men. The androgen receptor (AR) a ligand-activated transcription factor, constitutes the main drug target for advanced cases of the disease. However, a variety of other transcription factors and signalling networks have been shown to be altered in patients and to influence AR activity. The oncogenic transcription factor c-Myc has been studied extensively in multiple malignancies, but its impact on AR activity in prostate cancer remains elusive. In this study we assessed the impact of clinically relevant levels of c-Myc overexpression on AR activity and transcriptional output. We found that c-Myc and the AR share a substantial amount of binding sites, which exhibit enhancer-like characteristics. Interestingly, c-Myc overexpression altered global AR chromatin occupancy and antagonised a subset of androgen-induced genes. Furthermore, c-Myc overexpression modified histone marks, most notably H3K4me1 and H3K27me3. Lastly, we validated the antagonistic relationship between c-Myc and two AR target genes, KLK3 and GNMT, in patient samples.

2017-04-14 | GSE73994 | GEO

Genome-wide perturbations by miRNA map onto functional cancer pathways identifying regulators of chromatin modifiers

Project description:Genome-wide perturbations by miRNA map onto functional cancer pathways identifying regulators of chromatin modifiers Total RNA obtained from cancer cell lines transfected with miR-365-3p for 24 hours compared to controls.

2015-03-31 | E-GEOD-64020 | biostudies-arrayexpress

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data